Members of the herpes virus group have been strongly implicated in the etiology of several human tumors, such as Burkitt's lymphoma, nasopharyngeal carcinoma and carcinoma of the cervix. In addition, herpes viruses are thought to be causitive agents of tumors in monkeys, rabbits, guinea pigs, chickens and frogs. A characteristic of tumor cells is the loss of their normal growth control concurrent with changes in their interactions with normal cells in situ and in vitro. Since control of cell growth appears to be mediated at the level of the cell membrane, changes in the plasma membranes of tumor cells are expected. I have previously shown that infection of cells with herpes simplex virus results in changes in the chemical compositon of cell membranes in addition to the antigenic changes known to occur. My observations included the identification of specific changes in membrane proteins and glycoproteins which reflected differences in the social behavior (interaction of cells among themselves) of cells infected with different strains of herpes simplex virus. This work will be extended through a study of the viral gene and gene products that are responsible for these changes. This approach will consist of a genetic analysis of viral mutants that cause different changes in the social behavior of infected cells and a continuation of my biochemical analysis of HSV induced cell fusion.